Evidence map›Paper›PMID 26172294›Full record

ArticleOncotarget2015

NF-κB/RelA-PKM2 mediates inhibition of glycolysis by fenofibrate in glioblastoma cells.

Dongfeng Han, Wenjin Wei, Xincheng Chen, Yaxuan Zhang, Yingyi Wang, Junxia Zhang, Xiefeng Wang, Tianfu Yu, Qi Hu, Ning Liu and 1 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
3.0field-weighted citation impact, top 8% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

34 citing papers in PubMed, 53 citations in OpenAlex.

  1. Article
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  4. NFκB and JNK pathways mediate metabolic adaptation upon ESCRT-I deficiency.Cellular and molecular life sciences : CMLS · 2024
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 2 institutions in 1 country.

Dongfeng HanDepartment of Neurosurgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.
Wenjin WeiDepartment of Neurosurgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.
Xincheng ChenDepartment of Neurosurgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.
Yaxuan ZhangDepartment of Neurosurgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.
Yingyi WangDepartment of Neurosurgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.
Junxia ZhangDepartment of Neurosurgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.
Xiefeng WangDepartment of Neurosurgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.
Tianfu YuDepartment of Neurosurgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.
Qi HuDepartment of Neurosurgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.
Ning LiuDepartment of Neurosurgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.
Yongping YouDepartment of Neurosurgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.
Jiangsu Province Hospital · CNNanjing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aerobic glycolysis (production of lactate from glucose in the presence of oxygen) is a hallmark of cancer. Fenofibrate is a lipid-lowering drug and an agonist of the peroxisome proliferator-activated receptor alpha (PPARα). We found that FF inhibited glycolysis in a PPARα-dependent manner in glioblastoma cells. Fenofibrate inhibited the transcriptional activity of NF-κB/RelA and also disrupted its association with hypoxia inducible factor1 alpha (HIF1α), which is required for the binding of NF-κB/RelA to the PKM promoter and PKM2 expression. High ratios of PKM2/PKM1 promote glycolysis and inhibit oxidative phosphorylation, thus favoring aerobic glycolysis. Fenofibrate decreased the PKM2/PKM1 ratio and caused mitochondrial damage. Given that fenofibrate is a widely used non-toxic drug, we suggest its use in patients with glioblastoma multiforme (GBM).

Indexed as

AnimalsBlotting, WesternCarrier ProteinsCell Line, TumorFemaleFenofibrateGlioblastomaGlycolysisHumansHypoxia-Inducible Factor 1, alpha SubunitMembrane ProteinsMice, NudeMicroscopy, Electron, TransmissionMitochondriaNF-kappa BPPAR alphaCarrier ProteinsFenofibrateHIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitMembrane ProteinsNF-kappa BPPAR alphaThyroid Hormone-Binding ProteinsThyroid HormonesTranscription Factor RelAfenofibratePKM2PPARαRelAWarburg effect

Identifiers

PMID26172294
PMCPMC4694890
OpenAlexW1918931417

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.